The relationship between neurotrophic factors and CaMKII in the death and survival of retinal ganglion cells.
The scientific discourse relating to the causes and treatments for glaucoma are becoming reflective of the need to protect and preserve retinal neurons from degenerative changes, which result from the injurious environment associated with this disease. Knowledge, in particular, of the signal transduction pathways which affect death and survival of the retinal ganglion cells is critical to this discourse and to the development of a suitable neurotherapeutic strategy for this disease. The goal of this chapter is to review what is known of the chief suspects involved in initiating the cell death/survival pathways in these cells, and what still remains to be uncovered. The least controversial aspect of the subject relates to the potential role of neurotrophic factors in the protection of the retinal ganglion cells. On the other hand, the postulated triggers for signaling cell death in glaucoma remain controversial. Certainly, the restricted flow of neurotrophic factors has been cited as one possible trigger. However, the connections between glaucoma and other factors present in the retina, such as glutamate, long held to be a prospective culprit in retinal ganglion cell death are still being questioned. Whatever the outcome of this particular debate, it is clear that the downstream intersections between the cell death and survival pathways should provide important foci for future studies whose goal is to protect retinal neurons, situated as they are, in the stressful environment of a cell destroying disease. The evidence for CaMKII being one of these intersecting points is discussed.
Cooper
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NG
Department of Anatomical Sciences and Neurobiology, University of Louisville School of Medicine, Louisville, KY 40292, USA. nigelcooper@louisville.edu
Laabich
A
A
Fan
W
W
Wang
X
X
D000818:Animals; D019208:Brain-Derived Neurotrophic Factor / Q000235:genetics / Q000378:metabolism; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2 / Q000235:genetics / Q000378:metabolism*; D053148:Caspase 3 / Q000378:metabolism; D016923:Cell Death / Q000502:physiology*; D002470:Cell Survival / Q000502:physiology*; D018691:Excitatory Amino Acid Antagonists / Q000378:metabolism; D005901:Glaucoma / Q000378:metabolism / Q000473:pathology; D006801:Humans; D007527:Isoenzymes / Q000235:genetics / Q000378:metabolism; D016202:N-Methylaspartate / Q000378:metabolism; D009414:Nerve Growth Factors / Q000378:metabolism*; D010455:Peptides / Q000378:metabolism; D017440:Photoperiod; D016194:Receptors, N-Methyl-D-Aspartate / Q000378:metabolism; D012160:Retina / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D012165:Retinal Ganglion Cells / Q000166:cytology / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology
D019208:Brain-Derived Neurotrophic Factor; D018691:Excitatory Amino Acid Antagonists; D007527:Isoenzymes; D009414:Nerve Growth Factors; D010455:Peptides; D016194:Receptors, N-Methyl-D-Aspartate; C489863:myristoylated autocamtide-2-related inhibitory peptide; D016202:N-Methylaspartate; D054732:Calcium-Calmodulin-Dependent Protein Kinase Type 2; D053148:Caspase 3